Romani A, Scarpa A
Department of Physiology and Biophysics, Case Western Reserve University, School of Medicine, Cleveland, OH 44106.
FEBS Lett. 1990 Aug 20;269(1):37-40. doi: 10.1016/0014-5793(90)81113-3.
The addition of norepinephrine to perfused rat livers and to collagenase isolated hepatocytes induced a marked and dose-dependent magnesium efflux. The addition of beta-adrenergic receptor antagonists, but not alpha-antagonists, completely blocked the Mg2+ efflux. The Mg2+ efflux could also be induced by forskolin and by permeable cAMP analogues. By contrast, the addition of carbachol or vasopressin induced a Mg2+ influx into isolated hepatocytes. These results indicate that a significant Mg2+ efflux from liver cells can be induced through the beta-adrenergic receptors and that it is mediated through the cytosolic cAMP levels.
向灌注的大鼠肝脏和胶原酶分离的肝细胞中添加去甲肾上腺素会诱导显著的、剂量依赖性的镁外流。添加β-肾上腺素能受体拮抗剂而非α-拮抗剂可完全阻断镁离子外流。福斯高林和可渗透的环磷酸腺苷类似物也可诱导镁离子外流。相比之下，添加卡巴胆碱或血管加压素会诱导镁离子流入分离的肝细胞。这些结果表明，通过β-肾上腺素能受体可诱导肝细胞中大量镁离子外流，且其通过胞质环磷酸腺苷水平介导。
